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l phenylalanine/nekrosis
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Tumor necrosis factor-alpha primes pulmonary hemodynamic response to N-formyl-L-methionyl-L-leucyl-L-phenylalanine.
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We tested the hypothesis that tumor necrosis factor-alpha (TNF-alpha) primes the hemodynamic response to the neutrophil agonist N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) in lungs isolated from guinea pigs. Lungs were isolated from animals 18 h after injection of TNF-alpha (3.20 x 10(5)
4-Borono-2-18F-fluoro-L-phenylalanine PET for boron neutron capture therapy-oriented diagnosis: overview of a quarter century of research.
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4-10B-Borono-2-18F-fluoro-L-phenylalanine (18F-FBPA) was developed for monitoring the pharmacokinetics of 4-10B-borono-L-phenylalanine (10B-BPA) used in boron neutron capture therapy (BNCT) with positron emission tomography (PET). The
Pervanadate-induced nuclear factor-kappaB activation requires tyrosine phosphorylation and degradation of IkappaBalpha. Comparison with tumor necrosis factor-alpha.
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Tumor necrosis factor activates nuclear transcription factor kappaB (NF-kappaB) by inducing serine phosphorylation of the inhibitory subunit of NF-kappaB (IkappaBalpha), which leads to its ubiquitination and degradation. In contrast, pervanadate (PV) activates NF-kappaB and induces tyrosine
Suppressive effects of cyclosporin A and FK-506 on superoxide generation in human polymorphonuclear leukocytes primed by tumor necrosis factor alpha.
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Most previous studies have found no effects of cyclosporin A and FK-506 on active oxygen generation in human polymorphonuclear leukocytes. Recently various differences in biologic properties have been reported between unprimed peripheral blood human polymorphonuclear leukocytes and tissue or primed
Irradiation up-regulates CD80 expression through induction of tumour necrosis factor-alpha and CD40 ligand expression on B lymphoma cells.
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Previously, we reported that 100 Gy X-ray irradiation followed by 24 hr incubation up-regulates CD80 expression in murine B lymphoma cells, A20-2J. In the present study, we analysed the underlying mechanisms of such up-regulation using A20-HL cells derived from A20-2J cells. Irradiation of A20-HL
Tumour necrosis factor beta (lymphotoxin) inhibits locomotion and stimulates the respiratory burst and degranulation of neutrophils.
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The data presented here demonstrate that recombinant human tumour necrosis factor beta (rHuTNF beta; lymphotoxin) is a neutrophil modulator. The lymphokine inhibited the locomotion of neutrophils and augmented the neutrophil oxygen-dependent respiratory burst in response to
Effect of glutathione depletion on inhibition of cell cycle progression and induction of apoptosis by melphalan (L-phenylalanine mustard) in human colorectal cancer cells.
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Intracellular levels of glutathione have been shown to affect the sensitivity of cells to cell death-inducing stimuli, as well as the mode of cell death. We found in five human colorectal cancer cell lines (HT-29, LS-180, LOVO, SW837, and SW1116) that GSH depletion by L-buthionine-[S,R]-sulfoximine
Processing and release of tumor necrosis factor alpha.
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Tumor necrosis factor alpha (TNFalpha) is synthesized as a transmembrane precursor form that is proteolytically processed and released as the soluble mature form. In human monocytes and monocytic cell lines, the production, processing, and release of TNFalpha are co-induced by certain activators,
Regulation of the processing and release of tumor necrosis factor alpha in a human macrophage cell line.
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The proteolytic cleavage of a variety of membrane proteins, including pro-tumor necrosis factor alpha (pro-TNF-alpha), is induced by various reagents such as phorbol 12-myristate 13-acetate (PMA). In this study we generated a human macrophage cell line that constitutively produces TNF-alpha, and
Arachidonic acid promotes glutamate-induced cell death associated with necrosis by 12- lipoxygenase activation in glioma cells.
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Glutamate induced glutathione (GSH) depletion in C6 rat glioma cells, which resulted in cell death. This cell death seemed to be apoptosis through accumulation of reactive oxygen species (ROS) or hydroperoxides representing cytochrome c release from mitochondria and internucleosomal DNA
Membrane oxidative metabolism of human eosinophilic cell line EoL-1 in response to phorbol diester and formyl peptide: synergistic augmentation by interferon-gamma and tumor necrosis factor.
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Human eosinophilic cell line EoL-1 was studied using luminol-dependent chemiluminescence (CL) for the ability to produce a respiratory burst upon stimulation with 12-O-tetradecanoylphorbol-13-acetate (TPA) and N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). TPA, a potent activator of protein
Effects of tumour necrosis factor alpha and interleukin-1 alpha and beta on human neutrophil migration, respiratory burst and degranulation.
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Recombinant human tumour necrosis factor alpha (rHuTNF alpha) was shown to inhibit human neutrophil migration in the presence or absence of a chemotactic gradient generated with the tripeptide, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP), at doses of 20-100 U/10(6) cells. In contrast,
Tumor necrosis factor reduces cAMP production in rat microglia.
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cAMP has been reported to exert a neuroprotective role in several in vivo and in vitro models of brain pathologies, mainly by regulating microglial activation and orienting these cells toward a neuroprotective phenotype. In order to elucidate the intracellular pathways regulated by tumor necrosis
Treatment with N-tosyl-l-phenylalanine chloromethyl ketone after the onset of collagen-induced arthritis reduces joint erosion and NF-kappaB activation.
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N-tosyl-l-phenylalanine chloromethyl ketone (TPCK) is known to inhibit NF-kappaB activation and the expression of inflammation mediators in cultured cells. We measured the potential of TPCK to inhibit the pathogenesis of collagen-induced arthritis by blocking NF-kappaB activation. Arthritis was
Augmentation of the human monocyte/macrophage chemiluminescence response during short-term exposure to interferon-gamma and tumour necrosis factor-alpha.
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The effects of short-term (30 min) pre-incubation of human monocytes and macrophages (3-day cultured monocytes) with leucocyte-derived human interferon-gamma (IFN-gamma) and recombinant human tumour necrosis factor-alpha (rTNF-alpha) were examined. Pre-incubation of either monocytes or macrophages
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